title: Glycaemic control is positively associated with prevalent fractures but not with bone mineral density in patients with Type 1 diabetes.
abstract: OBJECTIVE
  There are conflicting data regarding the risk of osteoporosis in patients with Type 1 diabetes. We investigated an association between diabetes, bone mineral density and prevalent fractures.
  
  
  METHODS
  A single-centre, cross-sectional study of men and pre-menopausal women with Type 1 diabetes (n = 128) and a matched control group (n = 77) was conducted. The primary outcome measure was bone mineral density and secondary measures were markers of bone metabolism and prevalent fractures.
  
  
  RESULTS
  Hip and total body bone mineral densities were significantly lower in women with diabetes compared with control subjects. In men, no difference in bone mineral density was found. A multivariate regression analysis in women with diabetes revealed higher BMI as the strongest predictor of higher total hip, femoral neck and total body bone mineral density, whereas previous fractures were inversely associated with total hip bone mineral density and C-terminal telopeptide of type I collagen with total body bone mineral density. Poor long-term glycaemic control was not associated with low bone mineral density. Fracture frequency was higher in patients with diabetes compared with control subjects (1.64 vs. 0.62 per 100 patient-years; P < 0.05). In a multivariable model, long-term HbA(1c) control was associated with increased clinical fracture prevalence (OR 1.92; 95% CI 1.09-2.75) in those with diabetes.
  
  
  CONCLUSIONS
  Type 1 diabetes contributes to low bone mineral density in women. Previous fractures and low BMI were strong predictors of impaired bone mineral density and should therefore be considered in risk estimation. Fractures are more frequent in Type 1 diabetes. Long-term hyperglycaemia may account for impaired bone strength, independently from bone mineral density.
authors.affiliation: Department of Medicine III, University-Hospital Jena, Jena, Germany. thomas.neumann@med.uni-jena.de
authors.forename: T
authors.initials: T
authors.lastname: Neumann
authors.forename: A
authors.initials: A
authors.lastname: Sämann
authors.forename: S
authors.initials: S
authors.lastname: Lodes
authors.forename: B
authors.initials: B
authors.lastname: Kästner
authors.forename: S
authors.initials: S
authors.lastname: Franke
authors.forename: M
authors.initials: M
authors.lastname: Kiehntopf
authors.forename: C
authors.initials: C
authors.lastname: Hemmelmann
authors.forename: T
authors.initials: T
authors.lastname: Lehmann
authors.forename: U A
authors.initials: UA
authors.lastname: Müller
authors.forename: G
authors.initials: G
authors.lastname: Hein
authors.forename: G
authors.initials: G
authors.lastname: Wolf
mesh_terms: D015415:Biomarkers / Q000378:metabolism; D015519:Bone Density / Q000187:drug effects / Q000502:physiology*; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D005260:Female; D050723:Fractures, Bone / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D008159:Lumbar Vertebrae / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology*; D015995:Prevalence; D011859:Radiography; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D006442:Glycated Hemoglobin; C517652:hemoglobin A1c protein, human